Heparin Induced Thrombocytopeia (HIT)

Heparin Induced Thrombocytopeia (HIT)

1. HEPARIN INDUCED THROMBOCYTOPENIA (HIT) Dr. Sayeedur Rahman Khan Rumi [email protected] MD Cardiology Final Part Student NHFH & RI

2. Introduction Heparin is a widely used anticoagulant drug for the treatment and prevention of thromboembolic disorders Heparin may cause immune thrombocytopenia (a reduction in platelet count), or HIT HIT occurs in approximately 3%-5% of patients during or after UFH treatment for 5 days or more. The incidence is much lower, less than 1% during and after LMWH therapy. HIT can cause life- or limb-threatening thromboses

3. Heparin Induced Thrombocytopenia Heparin induced thrombocytopenia (HIT) is characterized by a decrease in the platelet count of more than 50% from the highest platelet count value after the start of heparin, an onset 5 to 10 days after the start of heparin, hypercoagulability, and the presence of heparin dependent, platelet activating IgG antibodies. HIT is an immune-mediated potentially fatal syndrome in which the heparin-induced immunoglobulins bridge platelets causing both thrombocytopenia and thrombosis. HIT does not induce bleeding but rather results in a paradoxical prothrombotic state. HIT is more common in surgical than medical patients (especially cardiac and orthopaedic patients).

4. 1. Increased platelet destruction Non-immune Septicemia/Inflammation Disseminated intravascular coagulation Thrombotic thrombocytopenic purpura Immune Autoimmune: idiopathic or secondary immune thrombocytopenia Alloimmune : post-transfusion purpura Drug-induced: prothrombic (heparin), prohemorrhagic (quinine, quinidine, gold, sulfa antibiotics, rifampin, vancomycin, NSAIDs, many others ) Clinical Conditions/Causes of Thrombocytopenia

5. Clinical Conditions/Causes of Thrombocytopenia (Cont‘d ) 2. Decreased platelet production Alcohol, cytotoxic drugs Aplastic anemia Leukemia, myelodysplasia Metastatic invasion of marrow Certain infections 3. Hypersplenism 4. Hemodilution (infusion of blood products, colloids, or crystalloids)

6. TYPES OF HIT

7. Parameter Type I HIT (non-immune mediated) Type II HIT (immune –mediated) Epidemiology 10-30% of UFH treated patients 1-5% of UFH-treated patients Less common with LMWH Temporal pattern Between days 1-4 of initiating UFH Between days 4-16 of initiating UFH/LMWH Severity of thrombocytopenia Mild, usually platelet counts remain > 100,000 Moderate to severe, mean platelet count 60,000 Antibody-mediated No Yes Thrombosis common No yes Management Observe Discontinue heparin/LMWH and start treatment with DTI Outcome Self-limited Death, arterial and venous thromb-osis are potential complications Immune vs Non Immune-Mediated HIT

8. Pathogenesis of Heparin-Induced Thrombocytopenia

9. Clinical events/ Complications associated with HIT Possible complications of HIT include the following: Deep venous thrombosis Pulmonary embolism Myocardial infarction Occlusion of limb arteries (possibly resulting in amputation) Transient ischemic attack and stroke Skin necrosis End-organ damage ( eg , adrenal, bowel, spleen, gallbladder, or hepatic infarction; renal failure) Death

10. Clinical signs of HIT Erythematous plaques Skin necrosis Deep venous thrombosis Venous gangrene

11. DIAGNOSIS OF HIT

12. Treatment of HIT The prompt cessation of heparin. As the condition is prothrombotic , these patients require alternative anticoagulation (In the United States, lepirudin , argatroban , and bivalirudin are licensed for HIT therapy) Prophylactic platelet transfusions should be avoided in patients with HIT. The risk of bleeding is very low, and such transfusions can increase the risk of thrombosis. The British Society of Haematology advises that all patients receiving prolonged heparin of any sort should have platelet counts on day 1 and every 2-4 days.

13. Thank you